R.S. Schwartz (Robert)http://repub.eur.nl/ppl/1613/
List of Publicationsenhttp://repub.eur.nl/eur_signature.pnghttp://repub.eur.nl/
RePub, Erasmus University RepositoryDo systemic risk factors impact invasive findings from virtual histology? Insights from the international virtual histology registryhttp://repub.eur.nl/pub/27706/
Fri, 01 Jan 2010 00:00:01 GMT<div>S. Philipp</div><div>D. Böse</div><div>W. Wijns</div><div>S.P. Marso</div><div>R.S. Schwartz</div><div>A. König</div><div>A. Lerman</div><div>H.M. Garcia-Garcia</div><div>P.W.J.C. Serruys</div><div>R. Erbel</div>
AimsCardiovascular risk factors such as elevated serum lipid levels are important in the development of coronary atherosclerosis. Radiofrequency (RF) analysis of intravascular ultrasound [IVUS, Virtual histology™ (VH)] offers a unique tool to study the composition of coronary atherosclerotic plaque in vivo. We used data from the multicentre VH registry to assess the association between cardiovascular risk factors and coronary plaque volume and composition.Methods and resultsBetween August 2004 and July 2006, 990 patients in 42 centres were enrolled in a prospective, multicentre, non-randomized global VH registry. Coronary artery imaging was performed by conventional IVUS and RF-IVUS. The four RF-IVUS plaque components [dense calcium (DC), necrotic core (NC), fibrous (F) tissue, and fibro fatty (FF)] were analysed in every recorded frame. The results were expressed as mean cross-sectional areas, absolute volume, and percentage of total plaque volume. Risk factor assessment included evaluation of family history of previous myocardial infarction (MI), past or current smoking, diabetes mellitus, hypertension, and the laboratory measurements. Patients with diabetes had an increased relative proportion of NC (6.47 ± 0.28 vs. 5.86 ± 0.14, P = 0.037) and DC (4.58 ± 0.27 vs. 3.90 ± 0.14, P = 0.017), and patients with hypertension had an increased relative proportion of FF, DC (4.35 ± 0.16 vs. 3.57 ± 0.17, P = 0.02) and NC (6.24 ± 0.17 vs. 5.60 ± 0.19, P = 0.01). Compared with patients with LDL-C <100 mg/dL, patients with LDL-C >160 mg/dL had higher plaque volume (342.1 ± 26.2 vs. 318.6 ± 10.7 mm3). Linear regression analysis showed a correlation between the level of HDL-C and F (r =-0.149, P < 0.01), FF (r =-0.106, P < 0.01), and NC (r =-0.90, P < 0.05). The level of LDL correlated with F (r = 0.110, P < 0.01). Patients with prior MI have an increased percentage of F (30.03 ± 0.59 vs. 28.20 ± 0.37, P = 0.009). Smoking had no relevant effect on plaque composition. Treatment with acetylsalicylacid and statins reduced FF with altering plaque volume.ConclusionRadiofrequency-IVUS detects marked differences in coronary plaque composition related to the risk factor profile with particular focus on lipid levels. Greater amounts of NC were associated with diabetes, hypertension, MI, and low HDL-C. The effects of treatment of changes related to plaque composition are underway.Imaging myocardial angiogenesishttp://repub.eur.nl/pub/27062/
Tue, 08 Sep 2009 00:00:01 GMT<div>J.J. Wykrzykowska</div><div>T.D. Henry</div><div>J.R. Lesser</div><div>R.S. Schwartz</div>
Imaging myocardial angiogenesis presents a major technical challenge because the ideal spatial resolution required is substantially higher than that available with standard X-ray angiography and nuclear medicine imaging. Moreover, these clinical imaging methods are currently inadequate (because of insufficient resolution) for clinical trials of angiogenic agents for the treatment of ischemic heart disease. Specialized techniques in MRI, ultrasonography, echocardiography and CT that are under development might provide improved means of imaging myocardial angiogenesis. Molecular imaging technologies are also being developed to improve resolution and to provide a better mechanistic insight into angiogenic therapies for ischemic heart diseases. This Review examines advanced methods for imaging angiogenesis. These technologies might soon permit data to be obtained directly from scientific studies and clinical trials.Synergistic Effect of Cardiovascular Risk Factors on Necrotic Core in Coronary Arteries. A Report From the Global Intravascular Radiofrequency Data Analysis Registryhttp://repub.eur.nl/pub/24418/
Fri, 01 May 2009 00:00:01 GMT<div>H.M. Garcia-Garcia</div><div>P.W.J.C. Serruys</div><div>G.S. Mintz</div><div>S. Saito</div><div>V. Klaus</div><div>P. Margolis</div><div>S.G. Carlier</div><div>D. Goedhart</div><div>R.S. Schwartz</div>
Objectives: This study explored whether an individual or a cluster of risk factors affects the extent of necrotic core (NC) assessed by intravascular ultrasound (IVUS) radiofrequency data (RFD) analysis. Background: Several systemic diseases contribute to the development of coronary artery disease. Methods: The Global Intravascular Radiofrequency Data Analysis Registry was a prospective, multicenter, nonrandomized database that enrolled 990 patients with coronary artery disease in whom 1 major coronary artery was imaged by IVUS-RFD. For the multivariable analysis, the population was divided into 4 classes: young women, young men (both ≤62 years), old women, and old men (>62 years). Mean NC area was categorized as 1: top quartile (≥0.62 mm2) or as 0: lower 3 quartiles. Results: Young patients had less NC compared with older patients (0.40 ± 0.36 mm2of NC vs. 0.50 ± 0.46 mm2in old patients, p = 0.0007). Nondiabetic patients had less NC than diabetic patients (0.43 ± 0.41 mm2of NC vs. 0.51 ± 0.44 mm2in diabetic patients, p = 0.02). The NC area was lower in normotensive patients (0.40 ± 0.36 mm2) than in hypertensive patients (0.48 ± 0.44 mm2) (p = 0.02). In the bivariate analysis, age, hypertension, diabetes, and prior coronary artery bypass graft were statistically significant, however in logistic regression analysis, only age (odds ratio [OR]: 1.023, 95% confidence interval [CI]: 1.009 to 1.037, p = 0.001) and diabetes (OR: 1.636, 95% CI: 1.174 to 2.279, p = 0.004) remained statistically significant. In a per-class logistic regression analyses including only diabetes as covariate, the OR in young women was 2.1 (95% CI: 0.77 to 6.0, p = 0.14), in young men the OR was 1.6 (95% CI: 0.90 to 2.7, p = 0.11), in old women the OR was 2.3 (95% CI: 1.09 to 4.9, p = 0.03), and in old men the OR was 1.6 (95% CI: 0.96 to 2.7, p = 0.07). Further, when only patients with diabetes and hypertension were included, young men (OR: 2.0, p = 0.041), old women (OR: 3.04, p = 0.046), and old men (OR: 2.2, p = 0.025) were significant. Conclusions: Individually and collectively, age and diabetes mellitus are associated with an increase in NC by IVUS-RFD analysis. Percutaneous recanalization of chronically occluded coronary arteries: a consensus document: part II.http://repub.eur.nl/pub/13947/
Tue, 18 Oct 2005 00:00:01 GMT<div>G.W. Stone</div><div>N.J. Reifart</div><div>I. Moussa</div><div>A. Hoye</div><div>D.A. Cox</div><div>A. Colombo</div><div>D.S. Baim</div><div>P.S. Teirstein</div><div>B.H. Strauss</div><div>M. Selmon</div><div>G.S. Mintz</div><div>O. Katoh</div><div>K. Mitsudo</div><div>T. Suzuki</div><div>H. Tamai</div><div>E. Grube</div><div>L.A. Cannon</div><div>D.E. Kandzari</div><div>M. Reisman</div><div>R.S. Schwartz</div><div>S.R. Bailey</div><div>G. Dangas</div><div>R. Mehran</div><div>J.W. Moses</div><div>M.B. Leon</div><div>P.W.J.C. Serruys</div><div>A.C. Abizaid</div>
Percutaneous recanalization of chronically occluded coronary arteries: a consensus document: part I.http://repub.eur.nl/pub/13937/
Tue, 11 Oct 2005 00:00:01 GMT<div>G.W. Stone</div><div>D.E. Kandzari</div><div>R. Mehran</div><div>A. Colombo</div><div>R.S. Schwartz</div><div>S.R. Bailey</div><div>I. Moussa</div><div>P.S. Teirstein</div><div>G. Dangas</div><div>D.S. Baim</div><div>M. Selmon</div><div>B.H. Strauss</div><div>H. Tamai</div><div>T. Suzuki</div><div>K. Mitsudo</div><div>O. Katoh</div><div>D.A. Cox</div><div>A. Hoye</div><div>G.S. Mintz</div><div>E. Grube</div><div>L.A. Cannon</div><div>N.J. Reifart</div><div>M. Reisman</div><div>J.W. Moses</div><div>M.B. Leon</div><div>P.W.J.C. Serruys</div><div>A.C. Abizaid</div>
Percutaneous recanalization of chronically occluded coronary arteries: Procedural techniques, devices, and resultshttp://repub.eur.nl/pub/58987/
Sat, 01 Oct 2005 00:00:01 GMT<div>G.W. Stone</div><div>A. Colombo</div><div>P.S. Teirstein</div><div>J.W. Moses</div><div>M.B. Leon</div><div>N.J. Reifart</div><div>G.S. Mintz</div><div>A. Hoye</div><div>D.A. Cox</div><div>D.S. Baim</div><div>B.H. Strauss</div><div>M. Selmon</div><div>I. Moussa</div><div>T. Suzuki</div><div>H. Tamai</div><div>O. Katoh</div><div>K. Mitsudo</div><div>E. Grube</div><div>L.A. Cannon</div><div>D.E. Kandzari</div><div>M. Reisman</div><div>R.S. Schwartz</div><div>S.R. Bailey</div><div>G. Dangas</div><div>R. Mehran</div><div>A.C. Abizaid</div><div>P.W.J.C. Serruys</div>
Recruitment of the androgen receptor via serum response factor facilitates expression of a myogenic genehttp://repub.eur.nl/pub/54437/
Fri, 04 Mar 2005 00:00:01 GMT<div>S. Vlahopoulos</div><div>W.E. Zimmer</div><div>G.W. Jenster</div><div>N.S. Belaguli</div><div>S.P. Balk</div><div>A.O. Brinkmann</div><div>R.B. Lanz</div><div>V.C. Zoumpourlis</div><div>R.S. Schwartz</div>
Androgen receptor (AR) induced precocious myogenesis in culture and myogenic specified gene activity. Increased levels of AR expression in replicating C2C12 myoblasts stimulated fusion into post-differentiated multinucleated myotubes and the appearance of skeletal α-actin transcripts, even in the absence of ligand. Furthermore, AR activated the skeletal α-actin promoter, which lacks GRE sites, in co-transfected C2C12 cells. AR co-activation of the skeletal α-actin promoter required co-expressed full-length serum response factor (SRF). In vitro, AR associated with SRF and was recruited by SRF to a α-actin promoter SRF binding site. Our data suggest that AR is capable of activating myogenic genes devoid of consensus AR binding sites via its recruitment by the myogenic enriched transcription factor, SHF.From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II.http://repub.eur.nl/pub/13247/
Tue, 14 Oct 2003 00:00:01 GMT<div>M. Naghavi</div><div>P. Libby</div><div>E. Falk</div><div>S.W. Casscells</div><div>S. Litovsky</div><div>J. Rumberger</div><div>J.J. Badimon</div><div>C. Stefanadis</div><div>P.R. Moreno</div><div>G. Pasterkamp</div><div>Z. Fayad</div><div>P.H. Stone</div><div>S. Waxman</div><div>P. Raggi</div><div>M. Madjid</div><div>A. Zarrabi</div><div>A.E. Burke</div><div>C. Yuan</div><div>P.J. Fitzgerald</div><div>D.S. Siscovick</div><div>C.L. de Korte</div><div>M. Aikawa</div><div>K.E. Juhani Airaksinen</div><div>G. Assmann</div><div>C.R. Becker</div><div>J.H. Chesebro</div><div>A. Farb</div><div>Z.S. Galis</div><div>C. Jackson</div><div>I.K. Jang</div><div>W. Koenig</div><div>R.A. Lodder</div><div>K. March</div><div>J. Demirovic</div><div>M. Navab</div><div>S.G. Priori</div><div>M.D. Rekhter</div><div>R. Bahr</div><div>S.M. Grundy</div><div>R. Mehran</div><div>A. Colombo</div><div>E. Boerwinkle</div><div>C. Ballantyne</div><div>W. Insull Jr</div><div>R.S. Schwartz</div><div>R. Vogel</div><div>P.W.J.C. Serruys</div><div>G.K. Hansson</div><div>D.P. Faxon</div><div>S. Kaul</div><div>H. Drexler</div><div>P. Greenland</div><div>J.E. Muller</div><div>R. Virmani</div><div>P.M. Ridker</div><div>D.P. Zipes</div><div>P.K. Shah</div><div>J.T. Willerson</div>
Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document will focus on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part I.http://repub.eur.nl/pub/13244/
Tue, 07 Oct 2003 00:00:01 GMT<div>M. Naghavi</div><div>P. Libby</div><div>E. Falk</div><div>S.W. Casscells</div><div>S. Litovsky</div><div>J. Rumberger</div><div>J.J. Badimon</div><div>C. Stefanadis</div><div>P.R. Moreno</div><div>G. Pasterkamp</div><div>Z. Fayad</div><div>P.H. Stone</div><div>S. Waxman</div><div>P. Raggi</div><div>M. Madjid</div><div>A. Zarrabi</div><div>A.E. Burke</div><div>C. Yuan</div><div>P.J. Fitzgerald</div><div>D.S. Siscovick</div><div>C.L. de Korte</div><div>M. Aikawa</div><div>K.E. Juhani Airaksinen</div><div>G. Assmann</div><div>C.R. Becker</div><div>J.H. Chesebro</div><div>A. Farb</div><div>Z.S. Galis</div><div>C. Jackson</div><div>I.K. Jang</div><div>W. Koenig</div><div>R.A. Lodder</div><div>K. March</div><div>J. Demirovic</div><div>M. Navab</div><div>S.G. Priori</div><div>M.D. Rekhter</div><div>R. Bahr</div><div>S.M. Grundy</div><div>R. Mehran</div><div>A. Colombo</div><div>E. Boerwinkle</div><div>C. Ballantyne</div><div>W. Insull Jr</div><div>R.S. Schwartz</div><div>R. Vogel</div><div>P.W.J.C. Serruys</div><div>G.K. Hansson</div><div>D.P. Faxon</div><div>S. Kaul</div><div>H. Drexler</div><div>P. Greenland</div><div>J.E. Muller</div><div>R. Virmani</div><div>P.M. Ridker</div><div>D.P. Zipes</div><div>P.K. Shah</div><div>J.T. Willerson</div>
Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document focuses on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.Artery size, neointima, and remodeling: time for some standards.http://repub.eur.nl/pub/4938/
Tue, 01 Dec 1998 00:00:01 GMT<div>R.S. Schwartz</div><div>E.J. Topol</div><div>P.W.J.C. Serruys</div><div>G. Sangiorgi</div><div>D.R. Holmes Jr</div>
Controversy continues regarding the mechanism of coronary restenosis. While neointimal thickening was initially considered the major cause, recent studies suggest that changes in arterial size, or remodeling, plays an important or even dominant role in late lumen loss. Moreover, neointimal thickness and remodeling may be interrelated. The field has been complicated by the fact that remodeling analyses have not used consistent definitions or methods. In this editorial we thus describe a quantitative paradigm for remodeling analyses: as arterial plaque or neointima forms in an artery, it is accompanied by luminal encroachment, artery expansion or gradations of either. In this manner, remodeling is generally defined as any arterial size change (enlargement or contraction), independent or dependent of neointimal thickening. Standardization of definitions and quantitative methods may improve understanding of the components of restenosis resulting from artery size changes, neointimal thickening and their impact on lumen size.Restenosis, reocclusion and adverse cardiovascular events after successful balloon angioplasty of occluded versus nonoccluded coronary arteries. Results from the Multicenter American Research Trial With Cilazapril After Angioplasty to Prevent Transluminal Coronary Obstruction and Restenosis (MARCATOR).http://repub.eur.nl/pub/5054/
Mon, 01 Jan 1996 00:00:01 GMT<div>P.B. Berger</div><div>D.R. Holmes Jr</div><div>E.M. Ohman</div><div>M.A. O'Hanesian</div><div>J.G. Murphy</div><div>R.S. Schwartz</div><div>P.W.J.C. Serruys</div><div>D.P. Faxon</div>
OBJECTIVES: This study sought to compare the frequency of restenosis, reocclusion and adverse cardiovascular events after angioplasty of occluded versus nonoccluded coronary arteries. BACKGROUND: Angioplasty of chronically occluded coronary arteries is believed to be associated with a higher frequency of restenosis and reocclusion than angioplasty of subtotal stenoses. Whether this leads to adverse cardiovascular events is unknown. METHODS: The Multicenter American Research Trial With Cilazapril After Angioplasty to Prevent Restenosis (MARCATOR) was a placebo-controlled trial with angiographic follow-up to determine the effect of the angiotensin-converting enzyme inhibitor cilazapril on the frequency of restenosis. In this trial, restenosis was defined as 1) angiographic reduction of minimal lumen diameter > or = 0.72 mm between angioplasty and the follow-up visit; and 2) > 50% diameter stenosis on the follow-up angiogram. We identified 139 patients with successful angioplasty of a coronary occlusion (Group 1) and compared the frequency of restenosis, reocclusion and adverse cardiovascular events with that in 1,295 patients with successful angioplasty of a subtotal stenosis (Group 2). RESULTS: Restenosis occurred in 36 patients with occluded arteries (29%) versus 264 with nonoccluded arteries (23%, p = 0.177) by definition 1 and in 62 patients with occluded arteries (49%) versus 478 with nonoccluded arteries (42%, p = 0.119) by definition 2. Occlusion was present in 24 Group 1 patients (19%) compared with 74 Group 2 patients (7%) (p < 0.001). During the 6 month follow-up period, two Group 1 patients (1.4%) and six Group 2 patients (0.5%) died; no Group 1 patients and 10 Group 2 patients (0.8%) developed severe congestive heart failure; nonfatal myocardial infarction occurred in 4 Group 1 patients (2.9%) and 31 Group 2 patients (2.4%); repeat coronary angioplasty or bypass surgery was performed in 29 Group 1 patients (21%) and 232 Group 2 patients (18%); and angina was present in 18 Group 1 and 163 Group 2 patients (13% for both). Eighty-six Group 1 patients (62%) and 853 Group 2 patients (66%) remained free of these adverse events during the 6-month follow-up period (p = 0.513). CONCLUSIONS: The frequency of restenosis was slightly but not significantly greater after successful angioplasty of an occluded artery than after angioplasty of a subtotal stenosis. Although reocclusion was more frequent, occurring in 19% of patients, the net clinical benefit of angioplasty in such patients was similar to that in patients with subtotal stenoses over the 6-month follow-up period.Restenosis, reocclusion and adverse cardiovascular events after successful balloon angioplasty of occluded versus nonoccluded coronary arteries: Results from the multicenter american research trial with cilazapril after angioplasty to prevent transluminal coronary obstruction and restenosis (MARCATOR)http://repub.eur.nl/pub/56515/
Mon, 01 Jan 1996 00:00:01 GMT<div>P.B. Berger</div><div>D.R. Holmes</div><div>E.M. Ohman</div><div>M.A. O'Hanesian</div><div>J.G. Murphy</div><div>R.S. Schwartz</div><div>P.W.J.C. Serruys</div><div>D.P. Faxon</div>